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R W Rosebrough

Publications and source records attributed to R W Rosebrough.

88 records · Page 5Linked to original sources

Effect of protein and amino acid status on lipogenesis by turkey poults.

Feeding trials were conducted with large White turkey poults to determine the role of dietary protein, sulfur amino acid (SAA), and lysine levels on growth and in vitro lipogenesis by turkey poults. A basal, 23% protein diet was formulated to contain 75% of the National Research Council (NRC) requirement for both SAA (8.0 g/kg) and lysine (12.9 g/kg). Lysine hydrochloride and L-methionine were added to the basal diet. A 30% protein diet was formulated to contain 100% of the requirement for SAA and lysine and served as the dietary control treatment. Twenty-three percent protein diets supplemented to contain the required levels of SAA (10.5 g/kg) and lysine (17.0 g/kg) supported growth and feed consumption equal to that attached with the control diet. Glutamic-aspartic amino transferase (GAT) and isocitrate dehydrogenase (ICD) activities were decreased (P less than 0.5) by 23% protein compared to 30% protein. Lysine additions to the 100% SAA diets increased GAT activity; however, additional lysine had little effect upon ICD activity. Each increment of lysine, whether fed to conjunction with 75 or 100% SAA, increased malic enzyme (ME) activity. It is suggested from the study that both GAT and ICD reflect the protein nutritional status of the poult and ME its lipogenic capacity. Lysine added to 23% protein diets increased (P less than .05) in vitro lipogenesis; however, this effect could be moderated by increasing the SAA level from 75 to 100% of the requirement. Liver slices preferentially used lactate over alanine as a lipid precursor; however, both lactate and alanine stimulated acetate incorporation into lipid equally. Liver slices did not use glucose for lipid synthesis to the degree that they used alanine, lactate, or acetate.

Acetates↗

Studies on the role of lysine and protein in the regulation of lipogenesis by the turkey poult.

Two feeding trials were conducted with Large White turkey poults to determine the role of lysine or protein level on growth and in vitro lipogenesis in turkey poults. Basal 23 and 30% protein diets were formulated with corn and soybean meal. Lysine HCl was added to the 23% protein diet in varying quantities. The soybean-to-corn meal ratio was adjusted in another series of diets to increase the lysine and protein levels. Growth and feed consumption were noted as functions of either lysine or protein levels. In vitro lipogenesis from alanine, lactate, or acetate was determined in the first experiment, whereas in vitro lipogenesis from acetate was determined in the presence of lactate or alanine in the second experiment. Lysine HCl increased (P less than .05) in vitro lipogenesis; however, increasing the lysine level with soybean meal decreased (P less than .05) lipogenesis. A great decrease in lipogenesis occurred when the protein level was increased from 25.3 to 26.8%. Lactate and alanine were used by liver tissue as substrates for lipogenesis and increased (P less than .05) lipogenesis from acetate.

Acetates↗

The role of carbohydrate and protein level in the regulation of lipogenesis by the turkey poult.

Three and 8-week feeding trials were conducted with Large White turkey poults to determine the role of dietary protein and carbohydrate levels on in vitro lipogenesis. In vitro lipogenesis was measured as nanomoles of sodium acetate incorporated into fatty acids per 100 mg of liver. A 23% protein-51% carbohydrate energy diet was selected as a lipogenic diet. Antilipogenic diets were formulated by adding fat at the expense of carbohydrate while the protein level (23%) was held constant. Antilipogenic diets were also formulated by holding the carbohydrate energy level at approximately 45% and increasing the protein level. When the carbohydrate energy level was held between 45 and 51% of the total energy content, increasing the protein level was held constant, decreasing carbohydrate energy decreased (P less than .05) in vitro lipogenesis. Dietary reversals were also conducted with 3 and 8-week-old poults. Poults consumed either the lipogenic diet (23% protein-51% carbohydrate energy) or the antilipogenic diets (24% protein-33% carbohydrate energy) for 3 and 8 weeks. At the end of each period, poults were switched for 3-day periods from lipogenic to antilipogenic diets and vice versa. At both age periods, the switch from lipogenic to antilipogenic diets decreased (P less than .05) lipogenesis whereas the opposite switch increased (P less than .05) lipogenesis. Diets containing 33% carbohydrate energy were more effective repressors of lipogenesis after 3 days than was the 30% protein-45% carbohydrate energy diet.

Animals↗

Effect of supplemental dietary chromium or nicotinic acid on carbohydrate metabolism during basal, starvation, and refeeding periods in poults.

A series of experiments were conducted with turkey poults to ascertain the effects of supplemental chromium or excess of nicotinic acid on growth and carbohydrate metabolism. A 23% protein starter diet was selected to emphasize the effect of chromium under basal, starvation for 48 hr, and refeeding periods. Thirty percent protein diets were also used to determine if the effects were compounded by protein levels. Supplemental chromium (20 ppm) significantly increased (P less than .05) weight at 3 weeks of age of poults consuming 23% protein diets, while an additional 250 ppm of nicotinic acid had little effect on poult weight at 3 weeks (P greater than .05). Supplemental chromium did not increase (P greater than .05) feed consumption of poults consuming both 23 and 30% protein diets. Supplemental chromium increased liver glycogen at 3 weeks of age and following refeeding after the 48 hr fast (P less than .05). Blood glucose was significantly affected by starvation-refeeding (P less than .05) but was not affected by either chromium or nicotinic acid. Supplemental chromium increased (P less than .01) active glycogen synthetase, while nicotinic acid increased (P less than .01) active phosphorylase at both protein levels. Synthetase was not decreased by starvation but was increased (P less than .01) by refeeding regardless of protein level fed. Phosphorylase was not affected by a starvation-refeeding regimen. Chromium supplementation increased in the vitro incorporation of (14C) glucose into glycogen during basal, starvation and refeeding periods (P less than .01), again, regardless of protein level.

Animal Feed↗

Effect of trivalent chromium on hepatic lipogenesis by the turkey poult.

Trivalent chromium (Cr+3) supplemented to a low-protein diet, 23% crude protein, significantly improved 21--day rate of gain of turkey poults. Hepatic lipogenesis from glucose was increased about 60% by Cr+3 supplementation. The majority of glucose incorporation was for fatty acid synthesis, although Cr+3 supplementation also enhanced synthesis of nonsaponifiable lipid and glycerol (P less than .01). The increased rates of lipogenesis by poults supplemented with Cr+3 did not affect liver lipid concentration. Starvation and refeeding induced a hyperlipogenic overshoot of glucose incorporation into fatty acids and glycerol. Chromium-supplemented poults had increased rates of fatty acid and glycerol synthesis from the glucose substrate, and increased concentration of liver lipid in comparison to control poults subjected to starvation and refeeding. Plasma concentration of free fatty acid was not affected by dietary treatment, but was reduced below basal values by starvation and refeeding (P less than .01). Plasma glucose level was not affected by dietary treatment or starvation, but was increased by refeeding (P less than .01). Apparently Cr+3 increased the rate of conversion of glucose to acetyl-CoA (glucose uptake).

Animal Feed↗

Effect of 1,3-butylene glycol on growth and in vivo and in vitro lipogenesis by turkey poults.

A series of feeding trials lasting 21 days was conducted with Large White turkey poults to determine the effects of 0, 12.5, and 25% energy as 1,3-butylene glycol (BG) on growth and on both in vivo and in vitro lipogenesis. The substitution of 12.5 and 25% of the energy as BG and on both in vivo and in vitro lipogenesis. The substitution of 12.5 and 25% of the energy as BG depressed growth and feed efficiency of 21-day-old poults (P less than 01). The relative liver size was increased by BG (P less than .01) while liver lipid per 100 g of body weight was decreased (P less than .01) by BG. IN vivo lipogenesis, determined by the incorporation of tritiated water into liver fatty acids was decreased (P less than .05) by BG. The evolvement of CO2 from both (1-14C) acetate and from (U-14C) glucose was decreased by BG. The results of this study indicate that while lipogenesis can be decreased by BG, growth is also decreased. Therefore, the regulation of growth parallels the regulation of lipid synthesis in the turkey poult.

Animals↗

Effects of dietary fat on feed efficiency, reproductive performance, and in vitro lipogenesis by the turkey hen.

Two 16-week feeding trials were conducted with Large White turkey hens to determine the effect of graded energy levels (as fat-6, 18, 30, and 42% substituted isocalorically for corn meal) on energy efficiency, reproductive performance, lipogenic enzyme activity, and in vitro lipogenesis. A constant calorie: gram-protein ratio (17:1) was maintained for all dietary treatments. Also, other components of the diets were adjusted to maintain constant energy-to-nutrient ratios. Additional fat increased (P less than .05) energy utilization but had no effect on reproductive performance. Additional fat calories decreased (P less than .05) malic enzyme, isocitrate dehydrogenase, and fatty acid synthetase activities; however, fatty acid synthetase activity was the most responsive of the three enzymes to 42% metabolizable energy as fat. Liver lipid content was also decreased (P less than .05) by additional fat calories. In vitro lipogenesis (fatty synthesis from 10 mM (1-14C) sodium acetate) was also decreased (P less than .01) by additional dietary fat.

Animal Feed↗

Effect of ketogenic diets in gestation on some characteristics of carbohydrate metabolism in fetal pig brain and liver.

Maternal ketosis was induced in sows by feeding 20% of the dietary energy as 1,3-butylene glycol (BG), medium-chain triglycerides (MCT), or a combination of the two. Brain development and hepatic glycogen synthetase and phosphorylase were assessed in 105-day-old fetuses as a function of maternal diets. Butylene glycol was more ketogenic than MCT. Furthermore, maternal ketosis induced by BG increased fetal brain weight, protein content, and cell size. Maternal ketosis also increased fetal liver glycogen possibly by causing the accumulation of glucose residues in the liver by suppressing liver glycolysis. In addition, glycogen synthetase alpha was increased by maternal ketosis. A fetal form of synthetase was noted in the liver which was stimulated by glucose-6-phosphate (G6P) in the presence of Na2SO4, an inhibitor of the G6P-dependent form of the enzyme.

3-Hydroxybutyric Acid↗

Effect of supplemental glucose or sucrose on liver and carcass glycogen metabolism of young chicks.

An experiment was conducted with Leghorn chicks to evaluate the effect of glucose or sucrose on liver and carcass glycogen. Phosphorylase a and synthase a were assayed to learn if glycogen cycle enzymes could be influenced by the early plane of nutrition. Both glucose and sucrose in drinking water increased liver and carcass glycogen in 3-day-old chicks. Groups given sucrose had more liver glycogen than groups given glucose after 5 days. Supplementary glucose given to fed chicks resulted in an increase in glycogen synthase a and a decrease in glycogen phosphorylase a at 4 days of age. By 6 days of age, differences in synthase activity between groups given sucrose or glucose were small. However, glucose solutions decreased phosphorylase a activity. The relationship between synthase a and phosphorylase a also partially regulates glycogen metabolism.

Age Factors↗

Control of glycogen metabolism in the developing turkey poult.

An experiment was conducted with young turkey poults to evaluate factors controlling glycogen metabolism in the period following hatching. Glucose and sucrose solutions were given along with a standard starter diet. Liver and carcass glycogen were measured on days 1, 4 and 6. Liver glycogen synthetase (EC 2.4.1.21) and phosphorylase (EC 2.4.1.1) were also assayed at these times. The characteristics of active and inactive glycogen synthetase at these times were determined and sensitivity of the active and inactive forms were related to physiological concentrations of glucose-6-phosphate. Supplemental glucose or sucrose increased carcass glycogen in comparison to controls; however, but sucrose was more effective than glucose in promoting liver glycogen synthesis in 4- and 6-day-old poults. There was an age dependent increase in carcass glycogen between days 1 and 6, but a decrease in liver glycogen between days 4 and 6. The activation of liver glycogen synthetase is incomplete in 1 day old poults but activity increases during the 1st week of life. Activation of glycogen synthetase decreased the apparent Ka for glucose-6-phosphate. Phosphorylase inactivation in vitro was not affected by age. Liver glucose-6-phosphate increases rapidly after hatching and the concentration is related to the in vitro Ka derived for both active and inactive synthetases. Both glucose and sucrose increased liver glucose-6-phosphate at days 4 and 6 as well as glycogen synthetase activity. The increase in enzyme activity may be caused indirectly by an allosteric effect of glucose-6-phosphate. Phosphorylase, while not affected by supplemental carbohydrates, did decrease in activity between days 4 and 6. The decrease in activity could affect the phosphorylase a/ synthetase a ratio and change glycogen metabolism.

Aging↗

Glycogen metabolism in the turkey embryo and poult.

Fertile eggs from Large White turkey hens were classified according to weight at time of incubation. Glycogen was measured in the 21-day-old embryo and one-day-old poult. Liver glycogen was positively correlated with initial egg weight in the 21-day-old embryo and negatively related to initial egg weight in the one-day-old poult. Glycogen recycling was evident in the one-day-old poult. Maximum accumulation of 14C-glucose as glycogen occurred 60 min post injection. Liver phosphorylase a level was higher in the one-day-old poult than the embryo. Total phosphorylase per gram of liver tissue was not different between the two age groups. Liver phosphorylase b was subject to conversion to phosphorylase a in both age groups. Avian phosphorylase exists in both the active and inactive form.

Animals↗

Glycogen depletion and repletion in the chick.

Carcass glycogen was degraded by chicks at a faster rate than liver glycogen during the first 72 hr of a 120 hr fast. Degradation of both sources of glycogen proceeded at a slower rate during the final 48 hr. Carcass glycogen was repleted at a greater rate than liver glycogen.

Animals↗

Effect of dietary energy on hepatic glycogen metabolism in the turkey hen.

An experiment was conducted with turkey hens to investigate the effect of substituting 30% of the carbohydrate calories with corn oil, 1,3-butanediol, or glycerol. Birds fed additional corn oil had the lowest liver glycogen concentration. Corn oil increased phosphorylase, a total phosphorylase, and glycogen synthetase I in comparison to the controls. Also, additional corn oil resulted in the highest specific activity of glucose-6-phosphatase. Dietary glycerol caused the highest concentration of liver glycogen. Glycerol increased glycogen synthetase I, but had little effect upon total activity in comparison to butanediol in the diet. Both butanediol and glycerol gave similar phosphorylase a activity, but butanediol increased total activity. The fat-fed and control-fed hens regulated hepatic glycogen concentration through phosphorylase, while glycerol and butanediol-fed hens regulated glycogen through glycogen synthetase. In vitro activation of glycogen synthetase I was deficient in hens fed additional corn oil, indicating a lack of glycogen synthetase phosphatase activity. The order of activation (glycerol greater than butanediol greater than control greater than corn oil) corresponds to the rank of glycogen concentrations

Animals↗

The effect of non-protein energy source and age on hexokinase concentration in chick muscle.

Muscle hexokinase was ascertained in the gastrocnemius muscles of 160 male chicks. Observations were made in four age groups and two diets. No differences in enzyme activity were observed which could be attributed to the feeding of either the high-carbohydrate or high-fat diet. Hexokinase activity declined significantly between 6 and 12 days of age in the chicks fed the respective diets.

Age Factors↗

The effect of non-protein energy sources on the ability of the chick to synthesize glucose-6-phosphatase.

Two experiments were conducted to investigate the relationship of energy source, age and glucose-6-phosphatase activity in the chick. In the first experiment liver glycogen and glucose-6-phosphatase were assayed in chicks of four age groups being fed either a high-fat or high-carbohydrate diet. It was observed that the feeding of the high-fat diet resulted in higher glucose-6-phosphatase activity and lower glycogen levels than did the feeding of the carbohydrate diet. Age was found to significantly influence enzyme activity. Both glucose-6-phosphatase and liver glycogen were found to be negatively correlated in the fat fed chicks. In the second experiment chicks were fed either a high-fat or high-carbohydrate diet for 28 days. Liver glucose-6-phosphatase activity was determined in representative samples of chicks from each group to establish basal levels. The diets were then reversed for a three-day period, after which the chicks were returned to their initial diets. Glucose-6-phosphatase was analysed at each step. Variation in enzyme activity in the chicks initially fed the high-fat diet could be attributed to differences in body weight. However, those chicks originally fed the carbohydrate diet did exhibit a true metabolic adaption when fed the high-fat diet.

Animals↗

The effect of non-protein energy source and age on the blood glucose level and the muscle glycogen content of young chicks.

Blood glucose levels and skeletal muscle glycogen concentrations were observed in 160 male chicks. Observations were made in four age groups and two diets. Carbohydrate diets resulted in higher blood glucose levels and glycogen concentrations than did fat diets. Age was found to significantly influence glycogen concentration in both diets. The linear regression of skeletal glycogen on blood glucose levels was significant in carbohydrate fed chicks.

Age Factors↗